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In JoVE (1)
Other Publications (2)
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Articles by Vincent Rouger in JoVE
رسم خرائط الانتشار الجزيئي في غشاء البلازما من قبل متعددة الهدف، للبحث عن المفقودين (MTT)
Vincent Rouger1,2,3, Nicolas Bertaux4,5,6, Tomasz Trombik1,2,3, Sébastien Mailfert1,2,3, Cyrille Billaudeau1,2,3, Didier Marguet1,2,3, Arnauld Sergé1,2,3
1Institut National de la Santé et de la Recherche Médicale, UMR 631, Parc scientifique de Luminy, 2Centre National de la Recherche Scientifique, UMR 6102, Parc scientifique de Luminy, 3Centre d'Immunologie de Marseille-Luminy, Aix-Marseille University, 4École Centrale Marseille, Technopôle de Château-Gombert, 5Institut Fresnel, Aix-Marseille University, 6Centre National de la Recherche Scientifique, UMR 6133, Aix-Marseille University
متعددة للبحث عن المفقودين الهدف هو خوارزمية محلية الصنع وضعت لتتبع الجزيئات بشكل فردي وصفت داخل الغشاء البلازمي للخلايا الحية. كشف بكفاءة، وتقدير وتعقب جزيئات مع مرور الوقت في كثافة عالية توفر سهل الاستعمال، وأداة شاملة للتحقيق في ديناميات غشاء النانو.
Other articles by Vincent Rouger on PubMed
Global/temporal Gene Expression in Diaphragm and Hindlimb Muscles of Dystrophin-deficient (mdx) Mice
American Journal of Physiology. Cell Physiology. Sep, 2002 | Pubmed ID: 12176734
The mdx mouse is a model for human Duchenne muscular dystrophy (DMD), an X-linked degenerative disease of skeletal muscle tissue characterized by the absence of the dystrophin protein. The mdx mice display a much milder phenotype than DMD patients. After the first week of life when all mdx muscles evolve like muscles of young DMD patients, mdx hindlimb muscles substantially compensate for the lack of dystrophin, whereas mdx diaphragm muscle becomes progressively affected by the disease. We used cDNA microarrays to compare the expression profile of 1,082 genes, previously selected by a subtractive method, in control and mdx hindlimb and diaphragm muscles at 12 time points over the first year of the mouse life. We determined that 1) the dystrophin gene defect induced marked expression remodeling of 112 genes encoding proteins implicated in diverse muscle cell functions and 2) two-thirds of the observed transcriptomal anomalies differed between adult mdx hindlimb and diaphragm muscles. Our results showed that neither mdx diaphram muscle nor mdx hindlimb muscles evolve entirely like the human DMD muscles. This finding should be taken under consideration for the interpretation of future experiments using mdx mice as a model for therapeutic assays.
Journal of Proteome Research. May, 2011 | Pubmed ID: 21410286
Duchenne muscular dystrophy (DMD) is caused by null mutations in the dystrophin gene, leading to progressive and unrelenting muscle loss. Although the genetic basis of DMD is well resolved, the cellular mechanisms associated with the physiopathology remain largely unknown. Increasing evidence suggests that secondary mechanisms, as the alteration of key signaling pathways, may play an important role. In order to identify reliable biomarkers and potential therapeutic targets, and taking advantage of the clinically relevant Golden Retriever Muscular Dystrophy (GRMD) dog model, a proteomic study was performed. Isotope-coded affinity tag (ICAT) profiling was used to compile quantitative changes in protein expression profiles of the vastus lateralis muscles of 4-month old GRMD vs healthy dogs. Interestingly, the set of under-expressed proteins detected appeared primarily composed of metabolic proteins, many of which have been shown to be regulated by the transcriptional peroxisome proliferator-activated receptor-gamma co-activator 1 alpha (PGC-1α). Subsequently, we were able to showed that PGC1-α expression is dramatically reduced in GRMD compared to healthy muscle. Collectively, these results provide novel insights into the molecular pathology of the clinically relevant animal model of DMD, and indicate that defective energy metabolism is a central hallmark of the disease in the canine model.